Traumatic aneurysm of the internal carotid artery in an infant: a surprise diagnosis

Case report

Traumatic aneurysm of the internal carotid arteryin an infant: a surprise diagnosis

NEIL CHAMBERS F R C A, M M E D, DARRYL HAMPSON-

EVANS F R C A, KIRAN PATWARDHAN M R C P, M R C P C H AND

LINDA MURDOCH F R C A

Departments of Anaesthesia and Paediatric Intensive Care, St George’s Healthcare NHS Trust,Tooting, London, UK

SummaryIsolated aneurysm of the extracranial section of the internal carotid

artery has been reported in children but never, to our knowledge, in

an infant. It can represent a major anaesthetic challenge with

compromise of both airway and cerebral perfusion and the associated

risks of rupture. We report on an 11-month-old infant, who had

undergone an examination under anaesthesia of her nose and throat

for epistaxis and gastrointestinal endoscopy due to apparent gastro-

intestinal bleeding shortly before presenting to us with signs of

rapidly progressive upper airway obstruction. Emergency examina-

tion under anaesthesia revealed a large pulsatile mass in the posterior

nasopharynx which, on subsequent radiological investigation, was

revealed to be a large pseudoaneurysm of the right internal carotid

artery, obstructing distal flow. An apparently minor episode of trauma

had occurred around the time of the first nosebleed; she had allegedly

fallen onto her face with a spoon in her mouth.

Keywords: neck aneurysm; carotid artery, internal; paediatric; airway

obstruction

Introduction

Upper airway obstruction in infants and toddlers

may be congenital or acquired. Congenital

abnormalities include choanal atresia, craniofacial

abnormalities, macroglossia, laryngeal or tracheal

lesions, tumours or cysts. These tend to present soon

after birth. Acquired causes include infective

processes, trauma, burns, inhaled foreign bodies,

tracheal stenosis, papillomas, haemangiomas,

mediastinal tumours, vascular rings, neurogenic

and immunological processes (1). Examination

under anaesthesia allows simultaneous diagnosis

of the underlying cause and securing of the airway.

We report a case of acute upper airway obstruction

in an infant with a surprising underlying cause,

which has significant implications for anaesthetic

and overall management.

Case report

An 11-month-old female infant, weighing 7.7 kg,

had been investigated for a 2-week history of

epistaxis, haematemesis and melaena at her district

hospital. She then presented to us with a 4-day

Correspondence to: Neil Chambers, Departments of Anaesthesiaand Paediatric Intensive Care, St George’s Healthcare NHS Trust,Tooting, London, UK.

Paediatric Anaesthesia 2002 12: 356–361

356 � 2002 Blackwell Science Ltd

history of increasing upper airway obstruction and

fatigue.

This previously healthy child had suffered five

episodes of epistaxis over the previous fortnight, all

resolving spontaneously. The second bleed had been

significant requiring admission, transfusion and

investigation at her local district hospital, 1 week

earlier. Examination under anaesthesia by the ear,

nose and throat team after this second bleed, using a

laryngeal mask airway (LMATM), had revealed no

source of the bleed and no obvious pathology. The

following day, she had undergone upper and lower

gastrointestinal endoscopy following an episode of

haematemesis and melaena in the ward. This inves-

tigation had also proved negative. Over the next few

days, she had suffered three further small episodes

of epistaxis.

She had then developed increasing stridor 4 days

prior to transfer to us, with several episodes of sleep

apnoea. There was no history of foreign body

inhalation. Since initial presentation, 2 weeks earlier,

the child had been generally well throughout, apart

from a mild upper respiratory tract infection. It was

noted that her first nosebleed had followed an

apparently minor tumble onto her face while she

had a spoon in her mouth; little attention had been

paid to this at the time.

Following transfer to us for management of the

airway obstruction, initial examination in the

ward revealed a tired, irritable infant, with some

drooling. She was sitting on her mother’s lap,

leaning forward with an extended chin and her

head was held slightly to the left. She had

marked inspiratory stridor and soft tissue recess-

ion. Subsequent examination made when the child

was falling asleep and supine showed almost

complete upper airway obstruction and recurrent

awakening, but without peripheral oxygen desat-

uration in room air. In spite of her distress, she

looked generally well, was apyrexial, not flushed

and was well hydrated on a dextrose saline

intravenous regime. There was no evidence of

active bleeding.

The child was given oral atropine as premedica-

tion and was brought urgently to theatre for an

endoscopic examination of the upper airway under

general anaesthesia. In theatre, the difficult airway

equipment, cross-matched blood and an ENT sur-

geon were present at induction.

Inhalational induction with oxygen, nitrous oxide

and sevoflurane was performed. A 20-gauge per-

ipheral cannula was inserted. Increasing airway

obstruction was overcome quite simply by chin lift,

head extension and the use of a small oropharyngeal

airway. Laryngoscopy revealed a pink mass in the

posterior nasopharynx and a full view of the larynx.

Orotracheal intubation was successfully achieved

without spraying the cords on deep inhalational

anaesthesia, using a size 4 tube, with the child

breathing spontaneously.

Endoscopic examination confirmed a large, pink

and pulsatile swelling near the right adenoid,

impinging on the tube, the posterolateral edges of

the epiglottis and the soft palate (Figure 1). There

was slight bleeding from the area of the mass. No

other abnormalities were found. The planned biopsy

was abandoned.

The child was then taken immediately to the CT

scanning department where a scan revealed a large,

Figure 1Laryngoscopic view of the aneurysm, with evidence of impinge-ment on the tracheal tube and of some active bleeding. Thetracheal tube is seen at the 1 o’clock position.

ANEURYSM OF THE INTERNAL CAROTID ARTERY 357

� 2002 Blackwell Science Ltd, Paediatric Anaesthesia, 12, 356–361

blood filled, thin walled mass measuring 4 ·3 · 3 cm, possibly aneurysmal in nature and

extending from the pyriform fossa to the posterior

nasopharynx. The mass compressed both the

intubated trachea and the right internal carotid

artery (Figures 2 to 5).

The child was then transferred to our paediatric

intensive care unit for sedation and ventilation

overnight to minimize the risk of catastrophic

haemorrhage by maintaining tight control of hae-

modynamic parameters and mechanical forces,

whilst further investigation and management was

planned. Specialized infant angiography at our

hospital is not available and so the origin or nature

of the mass could not be confirmed immediately.

The following day, the child was transferred to

Great Ormond St Children’s Hospital for further

neuroradiological assessment. Angiography con-

firmed an enormous saccular pseudoaneurysm of

the right internal carotid artery, with complete

obstruction of blood flow distally (with good con-

tralateral flow through the circle of Willis and flow

through the ipsilateral ophthalmic artery) (Figure 6).

An interdisciplinary decision was then taken to

embolize the right internal carotid artery using a

coil. This was achieved successfully by the cardiolo-

gists; she was then sedated and ventilated for a

further 3 days while her upper airway obstruction

diminished and she was then extubated. She was

discharged to the ward after a further 24 h.

In the ward she continued to have a few small

bleeds, decreasing both in volume and frequency. A

right-sided ‘Horner’s syndrome’ was noted, but

Figure 2Enhanced axial scan with the internal carotid artery aneurysmsituated between the tracheal tube (arrowhead) and the internal(long arrow) and external (short arrow) carotid arteries.

Figure 3Enhanced axial scan illustrating compression of the internalcarotid artery (long arrow) by the aneurysm (the short arrowindicates the thrombosed part of the aneurysm whereas thearrowhead indicates the lumen).

Figure 4Enhanced sagittal reformat scan showing the close proximity ofthe tracheal tube (long arrow) with the internal carotid arteryaneurysm (short arrow).

358 N. CHAMBERS ET AL.


otherwise she was neurologically intact. This was

probably neuropraxic in nature and was expected to

be temporary (2). She developed a femoral artery

thrombosis secondary to the angiography cannula

and could not be thrombolysed; fortunately, this

resolved spontaneously, but she may be at risk of

developing leg claudication in the future. She was

discharged home after a further 10 days.

Further imaging is due be undertaken over the

next few months to confirm permanent obliteration

of the right internal carotid artery and an absence of

contralateral backflow to the aneurysmal site.

Discussion

It is difficult to be absolutely certain of the aetiology

of this aneurysm: there was no real evidence of

infection, although the infant did have a mild upper

respiratory tract infection on admission. In fact,

nasal secretions cultured on admission grew Hae-

mophilus influenza, but there were no overt signs of

chest, neck or parapharyngeal infection. There was

the initially unremarkable history of tumbling onto a

spoon, causing minor trauma to the back of the

mouth around the time of her first nosebleed.

Additional evidence for a traumatic origin, however,

includes the rapid growth in size of the aneurysm,

the angiographic appearance of a saccular pseudo-

aneurysm and the absence of another explanation.

Oropharyngeal trauma in children has been

extensively documented; it is uncommon and

should raise the suspicion of nonaccidental injury

(3). Schoem et al. performed a retrospective analysis

of 26 children seen by an ENT team with documen-

ted oropharyngeal trauma over an 8-year period and

found none to have significant vascular injury (4).

Tostevin et al., however, reported a case of a med-

iastinitis and carotid sheath exposure in a toddler

following a fall onto a toothbrush and a case of

nonaccidental penetrating trauma to the oropharynx

in a 7-week-old infant causing exposure of the

carotid sheath (3). Sidhu et al. reported a case of

delayed neurological changes due to thrombosis of

the internal carotid artery (ICA) following a fall on to

a toothbrush in a 17-month-old (5). He proposed that

Figure 5Unenhanced axial scan at the level of the internal carotid arteryaneurysm (outlined by arrow heads), with evidence of some freshthrombus at the posterolateral aspect (arrow).

Figure 6Angiogram showing a large internal carotid aneurysm just distalto the bifurcation with little distal flow. There is good contralateralflow through the circle of Willis. The external diameter of theaneurysm may be underestimated because only the internaldiameter is shown, which may be further decreased by intralu-minal thrombus.



the mechanism of injury was probably sudden

compression of the artery between the intraoral

foreign object and the transverse processes of the

upper cervical spine causing stretching and shearing

of the intima, leading to thrombus propagation; this

child was successfully treated with anticoagulation

and made a full recovery.

Blunt carotid trauma from all causes in children

has been reviewed by Lew et al. and was found to be

very rare and usually associated with significant

other injury (6). Penetrating trauma, however, has

been reported previously as a cause of ICA

aneurysm in a 7-year-old child due to accidental

puncture, during myringotomy, of a lateral, aber-

rantly located artery (7).

Extracranial internal carotid artery aneurysms are

extremely rare in children: sporadic case reports do

exist, i.e. in a 3-year-old (2) and a 13-year-old (8), but

never before, to our knowledge, in an infant. Internal

carotid artery aneurysm in children may be true or

false, congenital (8) or acquired. Acquired causes

include infection (9), idiopathic (10), collagen diseases

(11,12) and spontaneous dissection (13). Cases in

adults have been reported secondary to apparently

minor trauma (14,15) and after penetrating trauma.

Posttraumatic ICA pseudoaneurysm, presenting with

epistaxis, has been described before in adults (16). As

mentioned above, traumatic pseudoaneurysm of the

internal carotid has been reported in an older child

with aberrant vasculature postmyringotomy. Presen-

tation of a traumatic pseudoaneurysm has not been

reported in this age group previously.

Presentation of extracranial internal carotid artery

aneurysm includes features of airway compromise

(2), a mass in the neck or nasopharynx (17), with

neurological signs: Horner’s syndrome (2), cranial

nerve palsies including recurrent laryngeal branch

of Vagus, features of cerebral infarction, i.e. ipsilat-

eral pain and contralateral weakness (18), with

epistaxis (14) or rupture (19).

Management may be conservative, surgical, poss-

ibly with external carotid artery bypass (20) or,

increasingly, by neuroradiological means. Neurolo-

gical defects after ligation/embolization of the

internal carotid artery are rare in children (21).

Several other issues are worthy of discussion.

Setting an LMA during the early management of this

infant increased the risk of iatrogenic bleeding. The

use of an LMA during investigation of supraglottic

airway obstruction is not ideal, in our opinion, and

may obscure the view of or cause trauma to a

developing mass.

The confusion over the source of blood loss meant

that upper and lower gastrointestinal bleeding was

suspected, due to swallowing of large amounts of

blood from the upper airway. Iatrogenic rupture of

the aneurysm at the time of upper gastrointestinal

endoscopy was therefore a very real possibility. In

addition, our own laryngoscopy and tracheal intu-

bation, during investigation and management of the

upper airway obstruction, also entailed a significant

risk of aneurysm rupture due to the haemodynamic

stress response in a relatively lightly anaesthetized

patient, and due to the risk of causing direct trauma

when unexpectedly dealing with a pulsatile mass

impeding airway visualization. The same risk of

trauma also applied to the use of other airway aids

(i.e. nasotracheal tubes, oral/nasopharyngeal air-

ways, Magill’s forceps or endoscopes).

There was also the question of the degree of

urgency of definitive management. With the rapidly

enlarging blood filled cavity so thin-walled and close

to the airway, there was some concern from the

surgical team that transfer or delay in definitive

management may be dangerous and urgent ‘on site’

exploration was initially discussed (without the

benefit of angiography, not available at our hospital

for such small children).

Another pitfall was deciding what levels of blood

pressure we should try to maintain in the intensive

care whilst awaiting further investigation. We were

unaware that cerebral perfusion was mainly

dependant on contralateral flow through the circle

of Willis. Induced hypotension to minimize risks of

aneurysm rupture could therefore have been inap-

propriate. Cerebral perfusion was challenged by

mechanical obstruction, the risk of rupture and

possible impairment of autoregulation. In adults

with intracranial carotid aneurysm, deliberately

invoking hypo- or hypertension may minimize the

risks and consequences of rupture or cerebral isch-

aemia, respectively. Due to the limited body of

experience in children, management of blood pres-

sure in order to optimize cerebral perfusion in such a

case remains largely speculative.

In spite of the potential for trouble, however, an

excellent result was achieved by providing good

basic anaesthetic care, maintaining normotension

360 N. CHAMBERS ET AL.


and arranging transfer for specialist neuroradiolog-

ical input.

Prior to definitive treatment, an occlusion test was

not performed in this case due to the risks of causing

further trauma to the dissected carotid artery; in

addition, good contralateral flow had been seen on

angiography. In adults, however, before a major

vessel ligation is performed, a noninvasive measure-

ment of cerebral blood flow may warn of the risk of

irreversible neurological injury. Single photon emis-

sion computed tomography, cerebral regional flow

using clearance of radioactive xenon or transcranial

Doppler, which evaluates middle cerebral artery

velocity and pulsatility, may assess global or regional

changes in blood flow during an occlusion test.

Additional considerations for anaesthesia for

future neuroangiographic studies in this child, to

assess the permanence of obliteration of the aneur-

ysmal sac, will include the potential for volume

overload and subsequent pulmonary oedema, sec-

ondary to the use of contrast. Also, there will be the

potential for diuresis and hypotension, raising the

question of the use of invasive monitoring during

the investigations.

A working diagnosis of a traumatic aetiology has

been made, following multidisciplinary discussions.

Possibly, a preexisting congenital weakness was

aggravated by minor trauma. Little literature exists

to help predict the medium or long-term risks for

this infant, who now essentially has a unilateral

blood supply to the brain. In addition, she is now

dependant on collateral arterial flow to the right leg.

Acknowledgements

We thank Mr H. Daya FRCS for the use of the

endoscopic photograph; Dr C. Peacock FRCR at the

Radiology Department at St George’s for the CT scans

and legends; and the Radiology Department at Great

Ormond Street for the use of their angiogram.

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Accepted 9 October 2001



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Traumatic aneurysm of the internal carotid artery in an infant: a surprise diagnosis